The effect of electronic cigarettes on young versus old normal hearts and pathologic hearts

电子烟对年轻与老年正常心脏和病理心脏的影响

基本信息

批准号：
10240296
负责人：
Robert A Kloner
金额：
$ 45.3万
依托单位：
HUNTINGTON MEDICAL RESEARCH INSTITUTES
依托单位国家：
美国
项目类别：
财政年份：
2018
资助国家：
美国
起止时间：
2018-09-14 至 2023-08-31
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/10240296
关键词：
Acrolein Acute Adolescent Adrenergic beta-Antagonists Adult Age Air Aldehydes Antioxidants Apoptosis Arrhythmia Arteries Atherosclerosis Biochemical Blood Pressure Cardiac Cardiac Catheterization Procedures Cardiovascular Diseases Cardiovascular Pathology Cardiovascular Physiology Cardiovascular system Cells Chemicals Chronic Cicatrix Cigarette Controlled Study Dangerousness Data Deterioration Dilatation - action Disease model Dose Echocardiography Electrocardiogram Electronic cigarette Endothelium Exposure to Female Fibrosis Flavoring Functional disorder Gene Expression Genotype Glycerol Goals Head Heart Heart Diseases Heart Rate Heart failure Histologic Human Hypertrophy Individual Infarction Inflammation Injury Knowledge Laboratories Left Left Ventricular Dysfunction Left Ventricular Function Left Ventricular Hypertrophy Left Ventricular Remodeling Long-Term Effects Lung Measures Mediating Mitochondria Modeling Morphology Myocardial Infarction Nicotine Outcome Particle Size Particulate Pathologic Phenotype Pilot Projects Pollution Propylene Glycols Rattus Reactive Oxygen Species Risk Rodent Rodent Model Smoke Stretching Structure Sympathetic Nervous System System Tars Testing Thinness Time Tobacco Toxic effect Vasodilation Ventricular aged cigarette smoke cigarette smoking effective therapy electronic cigarette use endothelial dysfunction experience heart function heart rate variability in vivo male mortality sex vaping vapor

项目摘要

Project Summary/Abstract E-cigarettes (E-C) continue to gain popularity, but the effects of E-C on the cardiovascular (CV) system of either normal individuals or those with heart disease are unknown. Cigarette smoke can increase heart rate, blood pressure, worsen endothelial dysfunction, and accelerate atherosclerosis. Some suggest that substituting E-C could be a safer approach to reduce cigarette smoking risks as they lack tar and some of the other noxious chemicals associated with cigarette smoke. However, E-C can still deliver nicotine and other potentially dangerous chemicals such as acrolein, propylene glycol, glycerol, aldehydes, and flavorings. In addition, the small particle size that may result from E-C vaping could result in increased toxicity to the lungs and cardiovascular system. There is a large knowledge gap in that there are no studies that have examined the effect of chronic exposure to E-C on the CV system in otherwise healthy young individuals where there has been a rapid increase in E-C use versus older individuals who may be turning to E-C as a way to quit standard cigarettes. In addition there is not data on the long-term effect of E-C on subjects with known CV disease. Thus, before suggesting that individuals can feel safe that their use of E-C is not going to cause or exacerbate CV disease, rigorous controlled studies are needed to assess the effect of E-C on CV phenotype and genotype. Our goal will be to determine the acute and chronic effects that E-C has in comparison to standard cigarette smoke on the young versus the old CV system and on the diseased CV system, including left ventricular (LV) dysfunction due to previous myocardial infarction (MI). We will determine whether E-C are safer, equally safe or less safe for subjects who have these underlying CV conditions versus standard cigarettes. We hypothesize that E-C, especially if they carry nicotine, will contribute to adverse LV remodeling post myocardial infarction, worsen heart failure, and endothelial dysfunction. We will determine whether these effects will be lessened if E-C does not contain nicotine, and whether certain therapies can reverse the effects. A well-established rodent model of MI will be used and there will be collaborative effort between a laboratory that has extensive experience subjecting rodents to exposure to smoke and pollution with a laboratory that has extensive experience with analyzing the pathophysiology of in vivo cardiac disease models including assessment by echocardiography, cardiac catheterization, detailed histologic and histochemical analyses, biochemical analyses, assessment of endothelial function, assessment of mitochondrial function, ultrastructural analysis, and assessment of gene expression.

项目概要/摘要电子烟（E-C）持续流行，但E-C对心血管（CV）系统的影响正常人还是患有心脏病的人尚不清楚。香烟烟雾会增加心率、血压，恶化内皮功能障碍，加速动脉粥样硬化。一些表明替代 E-C 可能是降低吸烟风险的更安全方法，因为它们缺乏焦油和其他一些与香烟烟雾有关的有毒化学物质。不过E-C还是可以的输送尼古丁和其他潜在危险的化学物质，如丙烯醛、丙二醇、甘油、醛类和香料。此外，E-C 电子烟可能产生的小颗粒尺寸可能会导致导致肺部和心血管系统的毒性增加。存在很大的知识差距没有研究检验长期暴露于 E-C 对 CV 系统的影响与老年人相比，其他方面健康的年轻人的 E-C 使用量迅速增加可能转向 E-C 作为戒烟方式的个人。另外没有数据 E-C 对患有已知 CV 疾病的受试者的长期影响。因此，在建议之前个人可以放心，他们使用 E-C 不会导致或加剧 CV 疾病，严格需要对照研究来评估 E-C 对 CV 表型和基因型的影响。我们的目标将确定 E-C 与标准香烟烟雾相比的急性和慢性影响年轻与年老 CV 系统以及患病 CV 系统（包括左心室 (LV)）的影响由于先前的心肌梗死（MI）而导致功能障碍。我们将确定E-C是否更安全，对于具有这些潜在心血管疾病的受试者，与标准受试者相比，同样安全或不太安全香烟。我们假设 E-C，特别是如果它们携带尼古丁，将导致不良的 LV 心肌梗塞后重塑，加重心力衰竭和内皮功能障碍。我们将确定如果 E-C 不含尼古丁，这些影响是否会减轻，以及是否某些疗法可以逆转效果。将使用完善的 MI 啮齿动物模型，并且将有具有丰富啮齿动物暴露经验的实验室之间的合作努力实验室在分析烟雾和污染方面拥有丰富的经验体内心脏病模型的病理生理学，包括超声心动图评估、心脏疾病导管插入术、详细的组织学和组织化学分析、生化分析、评估内皮功能、线粒体功能评估、超微结构分析和评估基因表达。

项目成果

期刊论文数量（3）

专著数量（0）

科研奖励数量（0）

会议论文数量（0）

专利数量（0）

Marijuana and electronic cigarettes on cardiac arrhythmias.

大麻和电子烟对心律失常的影响。

DOI：
10.1016/j.hrthm.2022.09.022
发表时间：
2023
期刊：
Heart rhythm
影响因子：
5.5
作者：
Kloner,RobertA
通讯作者：
Kloner,RobertA

E-cigarette or Vaping Product Use-Associated Lung Injury Produced in an Animal Model From Electronic Cigarette Vapor Exposure Without Tetrahydrocannabinol or Vitamin E Oil.

DOI：
10.1161/jaha.120.017368
发表时间：
2020-09-15
期刊：
Journal of the American Heart Association
影响因子：
5.4
作者：
Kleinman MT;Arechavala RJ;Herman D;Shi J;Hasen I;Ting A;Dai W;Carreno J;Chavez J;Zhao L;Kloner RA
通讯作者：
Kloner RA

One Acute Exposure to E-Cigarette Smoke Using Various Heating Elements and Power Levels Induces Pulmonary Inflammation.